Engineering of N-Acyl Homoserine Lactone (AHL) genes in the quorum-sensing of Pseudomonas

Hundreds of millions of patients every year acquire nosocomial infections according to the World Health Organisation. Treatment is complicated by antibiotic resistance with a rapid increase of multi-drug resistance (MDR) bacteria, including strains of the gram-negative genera: Pseudomonas and Escherichia. Opportunistic Pseudomonas are responsible for 10% of all global nosocomial infections in immunocompromised individuals with 50-90% of patients of cystic fibrosis patients suffering from a Pseudomonas Aeruginosa infection. A major contributor to antibiotic resistance is bacterial aggregation to form biofilms. Bacteria within biofilms communicate through chemicals, such as N-Acyl homoserine lactones (AHL), quorum-sensing molecules essential to biofilm formation. We aim to develop strategies to inhibit biofilm formation by targeting AHL regulation genes: ppuR, ppuA, ppuI and RsaL in Pseudomonas putida. This project has a vast range of potential therapeutic applications such as the development of biocontainment devices and will provide fundamental information to understanding and developing tools in combating antibiotic resistance.